The JNK signaling pathway mediates the progression of CKD by participating in inflammation, fibrosis, oxidative stress, and nephrotoxicity.[23] Studies have shown that G2/M blockade in renal tubular epithelial cells activates the JNK signaling pathway and promotes fibroblast factor secretion; blocking JNK signaling pathway activation inhibits TGF-β1-mediated renal fibrosis.[24,25] The role of the TGF-β signaling pathway in the pathogenesis of CKD has been researched. This evidence concerns the gene TGFB1 and chronic kidney disease.